Hippocampal Input to the Nucleus Accumbens Shell Enhances Food Palatability

Yang, Angela K.; Mendoza, Jesse A.; Lafferty, Christopher K.; Lacroix, Franca; Britt, Jonathan P.

doi:10.1016/j.biopsych.2019.09.007

Cited by 30 publications

(24 citation statements)

References 80 publications

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“…Several excitatory inputs to the NAc are involved in feeding behavior [10][11][12][13] . We chose to investigate the role of NAc inputs from the aPVT and PFC because they both appear to regulate the consumption of drugs of abuse and palatable food yet have distinct reinforcing properties when acutely activated [14][15][16][17][18][19] .…”

Section: Resultsmentioning

confidence: 99%

Input-specific modulation of murine nucleus accumbens differentially regulates hedonic feeding

et al. 2021

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Hedonic feeding is driven by the “pleasure” derived from consuming palatable food and occurs in the absence of metabolic need. It plays a critical role in the excessive feeding that underlies obesity. Compared to other pathological motivated behaviors, little is known about the neural circuit mechanisms mediating excessive hedonic feeding. Here, we show that modulation of prefrontal cortex (PFC) and anterior paraventricular thalamus (aPVT) excitatory inputs to the nucleus accumbens (NAc), a key node of reward circuitry, has opposing effects on high fat intake in mice. Prolonged high fat intake leads to input- and cell type-specific changes in synaptic strength. Modifying synaptic strength via plasticity protocols, either in an input-specific optogenetic or non-specific electrical manner, causes sustained changes in high fat intake. These results demonstrate that input-specific NAc circuit adaptations occur with repeated exposure to a potent natural reward and suggest that neuromodulatory interventions may be therapeutically useful for individuals with pathologic hedonic feeding.

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Section: Resultsmentioning

confidence: 99%

Input-specific modulation of murine nucleus accumbens differentially regulates hedonic feeding

et al. 2021

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“…For example, in this scenario ghrelin could indirectly activate ghrelin-sensing LH neurons that then promotes VTA activity (Cone et al, 2014(Cone et al, , 2016 to provide a dopaminergic input to hippocampus. Other potential neuromodulators or neuropeptides that could act as co-agonists to ghrelin signalling in vS include acetyl-choline from septal areas (Colgin et al, 2003), serotonin from raphe (Yang et al, 2020) or melanin concentrating hormone from hypothalamus (Noble et al, 2019).…”

Section: Mechanisms Of Ghrelin Signalling In Vsmentioning

confidence: 99%

“…Similarly, a separate population of neurons projecting to the lateral hypothalamus (LH) have been shown to be recruited during salient environments and during learning of food associations (Hsu et al, 2015;Jimenez et al, 2018;Mohammad et al, 2021). Both of these populations of neurons are therefore well placed to control anticipatory feeding related behaviour (Hsu et al, 2015;Reed et al, 2018;Yang et al, 2020). While this makes vH ideally placed to powerfully control motivational and hunger-related behaviour, each population has distinct influence on ongoing behaviour (AlSubaie et al, 2021;Britt et al, 2012;Hsu et al, 2015;Jimenez et al, 2018;LeGates et al, 2018;Mohammad et al, 2021;Trouche et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Internal state dependent control of feeding behaviour via hippocampal ghrelin signalling

Mishchanchuk

AlSubaie

MacAskill

2021

Preprint

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Hunger is an internal state that not only invigorates behaviour towards feeding, but also acts as a contextual cue for the higher-order control of anticipatory feeding-related behaviour. The ventral hippocampus is a brain region important in encoding context, but how internal contexts such as hunger are represented in hippocampal circuits is not known. Pyramidal neurons in the ventral hippocampus, and in particular within the ventral CA1/subiculum border (vS) express the receptor for the peripheral hunger hormone ghrelin, and ghrelin is known to cross the blood brain barrier and directly influence hippocampal circuitry. However, what role vS neurons play during feeding related behaviour, and how ghrelin influences this role has not been directly investigated. In this study, we used a combination of whole-cell electrophysiology, optogenetics and molecular knockdown together with in vivo calcium imaging in mice to investigate the role of vS during feeding behaviour across different states of hunger. We found that activity of a unique subpopulation of vS neurons that project to the nucleus accumbens (vS-NAc) were active specifically when animals approached and investigated food, and that that this activity inhibited the transition to begin eating. Increases in peripheral ghrelin reduced vS-NAc activity during this anticipatory phase of feeding behaviour, by increasing the influence of synaptic inhibition. Furthermore, this effect required postsynaptic GHSR1a expression in vS-NAc neurons, suggesting a direct role of ghrelin signalling. Consistent with this role of hippocampal ghrelin signalling, removal of GHSR1a from vS-NAc neurons impaired ghrelin-induced changes in feeding-related behaviour. Together, these experiments define a ghrelin-sensitive hippocampal circuit that informs the decision to eat based on internal state.

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“…As HL participants rated the negative social feedback videos as more pleasant than the control participants, reduced NAcc responses to negative social feedback might thus reflect reduced tendencies to avoid this negative social feedback. Furthermore, the enhanced functional coupling of the NAcc with a hippocampal cluster that correlated with individual pleasantness ratings is in line with the involvement of this neural circuit in hedonic processing [63] and might reflect the rewarding experience of a social feedback for socially deprived individuals [64]. Nevertheless, we have recently found a compromised neural integration of social information in HL participants evident in various brain regions including the NAcc [37].…”

Section: Discussionmentioning

confidence: 65%

Behavioral and neural dissociation of social anxiety and loneliness

Lieberz

Shamay‐Tsoory²,

Saporta³

et al. 2021

Preprint

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Loneliness is a public health concern with detrimental effects on physical and mental well-being. Given phenotypical overlaps between loneliness and social anxiety, cognitive behavioral interventions targeting social anxiety might be adopted to reduce loneliness. However, it is still elusive whether social anxiety and loneliness share the same underlying neurocognitive mechanisms. The current study aimed at investigating to what extent known behavioral and neural correlates of social avoidance in social anxiety are evident in loneliness. We used a pre-stratified approach involving 42 participants with high and 40 control participants with low loneliness scores. During functional magnetic resonance imaging (fMRI), the participants completed a social gambling task to measure the subjective value of engaging in a social situation and responses to positive and negative social feedback. Uni- and multivariate analyses of behavioral and fMRI data replicated known task effects across groups. However, although lonely participants were characterized by increased social anxiety, loneliness was associated with a response pattern clearly distinct from social anxiety. Specifically, Bayesian analyses revealed moderate evidence for equal subjective values of engaging in social situations and comparable amygdala responses to social decision-making and striatal responses to positive social feedback in both groups. Conversely, lonely participants showed significantly altered behavioral responsiveness to negative feedback and opposing striatal brain activity and connectivity compared to controls. Our findings suggest that loneliness is associated with altered emotional reactivity to social situations rather than behavioral tendencies to withdraw from social interactions. Thus, established interventions for social anxiety should be adjusted when targeting loneliness.

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Hippocampal Input to the Nucleus Accumbens Shell Enhances Food Palatability

Cited by 30 publications

References 80 publications

Input-specific modulation of murine nucleus accumbens differentially regulates hedonic feeding

Input-specific modulation of murine nucleus accumbens differentially regulates hedonic feeding

Internal state dependent control of feeding behaviour via hippocampal ghrelin signalling

Behavioral and neural dissociation of social anxiety and loneliness

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